Expression of transforming growth factor alpha in experimental gastric carcinogenesis.

Livingstone, J. I.; Filipe, M. I.; Wastell, C

doi:10.1136/gut.35.5.604

Cited by 11 publications

(11 citation statements)

References 13 publications

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“…Livingstone et al (1994) found that the carcinogen MNNG significantly increased the intensity of TGF-α expression in the gastric mucosa and in adenocarcinomas. TGF-α is a 50-amino-acid peptide first isolated from fibroblasts transformed by rodent sarcoma viruses (De Larco and Todaro, 1978) which acts as a ligand for the epidermal growth factor receptor (Derynck, 1986).…”

Section: Discussionmentioning

confidence: 99%

“…Immunohistochemistry was performed with the mouse monoclonal antibody AB-2 (Oncogene Science, Cambridge, UK), which is specific for human and rat TGF-α and exhibits no crossreactivity to epidermal growth factor (Livingstone et al, 1994). Sections were predigested with trypsin for 15 min to expose the antigenic sites before incubation with AB-2 at a dilution of 5:100 overnight at 4°C.…”

Section: Immunohistochemical Observation Of Tgf-αmentioning

confidence: 99%

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Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

et al. 1999

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The effect of prolonged administration of all- trans -retinoic acid (RA) on sodium chloride-enhanced gastric carcinogenesis induced by N -methyl- N ′-nitro- N -nitrosoguanidine, and the labelling and apoptotic indices and immunoreactivity of transforming growth factor (TGF) α in the gastric cancers was investigated in Wistar rats. After 25 weeks of carcinogen treatment, the rats were given chow pellets containing 10% sodium chloride and subcutaneous injections of RA at doses of 0.75 or 1.5 mg kg −1 body weight every other day. In week 52, oral supplementation with sodium chloride significantly increased the incidence of gastric cancers compared with the untreated controls. Long-term administration of RA at both doses significantly reduced the incidence of gastric cancers, which was enhanced by oral administration of sodium chloride. RA at both doses significantly decreased the labelling index and TGF-α immunoreactivity of gastric cancers, which were enhanced by administration of sodium chloride, and significantly increased the apoptotic index of cancers, which was lowered by administration of sodium chloride. These findings suggest that RA attenuates gastric carcinogenesis, enhanced by sodium chloride, by increasing apoptosis, decreasing DNA synthesis, and reducing TGF-α expression in gastric cancers. © 1999 Cancer Research Campaign

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Section: Discussionmentioning

confidence: 99%

Section: Immunohistochemical Observation Of Tgf-αmentioning

confidence: 99%

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

et al. 1999

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“…positivity to TGF-α in gastric mucosa from normal rats (Livingstone et al, 1994;Montaner et al, 1999) and humans Abe et al, 1997). Accordingly, TGF-α mRNA, but not EGF mRNA, was shown to be expressed in the normal stomach from several species (Beauchamp et al, 1989;Malden et al, 1989).…”

Section: A B C Dmentioning

confidence: 99%

“…However, at present data concerning the localization of TGF-α and its receptor in the upper digestive tract of the rat are lacking and discordant. For example, Livingstone et al (1994) and Hormi et al (1995) found a different distribution of TGF-α immunopositivity between fundic (cardiac) and antral mucosa in rat stomach, these data being criticized by Montaner et al (1999). In any case, in all these studies the immunolocalization of TGF-α in the rat gastroduodenal area was evaluated only on the basis of the examination of a few gastric mucosal samples (Livingstone et al, 1994;Montaner et al, 1999), then an accurate determination of distribution and localization of TGF-α in the whole gastric mucosa are not available.…”

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confidence: 99%

Differential distribution of transforming growth factor-a immunohistochemistry within whole gastric mucosa in rats

Natale¹,

Lazzeri²,

Blandizzi³

et al. 2009

Eur J Histochem

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Transforming growth factor-α (TGF-α) plays an important role in both proliferation and differentiation of mucosal cells at the gastrointestinal level, including stomach, where it is constitutively produced. This study evaluated the immunohistochemical distribution of TGF-α within whole gastric mucosa in rats, through the examination of seriate sections. Each stomach was opened along the greater curvature, pinned upon a cork plate, fixed in formalin and cut in 2-mm parallel strips which were sequentially superimposed on a glass slide. Sections were immunostained for TGF-α and pictures were taken from three areas: greater and lesser curvature; mucosa lying between the two curvatures. The sections were graded on the basis of the intensity of TGF-α staining, which was scored as follows: 0) no staining; 1) weakly positive; 2) intensely positive. The percent number of immunopositive cells and a mean intensity were calculated. Gastric mucosa showed a marked immunopositivity to TGF-α, mainly in parietal cells whose cytoplasm displayed moderate to intense staining. Positive cells (and the mean intensity) of total mucosa were 15.7±6.1% (1.13±0.42). However, they were not uniformly distributed, being 26.3±1.9% (1.67±0.24) in the mucosa lying between the two curvatures, 12.4±2.5% (1.52±0.22) along the lesser curvature and 8.3±2.1% (0.31±0.17) along the greater curvature. These results show that parietal cells of rat gastric mucosa exhibit immunoreactivity to TGF-α. Considering the gastroprotective effects of this factor, its non-homogeneous distribution within different areas may be of importance in understanding the lesion pattern of gastric damage after the administration of noxious agents.

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“…In addition, environmental factors significantly contribute to the etiology of cancer [2] . N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is commonly used to induce gastric tumors in basic research [8,9] , therefore we chose MNNG to induce gastric precancerous leisions and gastric tumors in this study. Consistent with other tumors, the pathogenesis of gastric tumors is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Expression of p-STAT3 and vascular endothelial growth factor in MNNG-induced precancerous lesions and gastric tumors in rats

Wang¹,

Wang²,

Zheng³

et al. 2016

WJGO

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Author contributions: Wang XY and Wang LL are co-first authors; they contributed equally to the work; Zheng X, Meng LN, Lyu B and Jin HF contributed to the conception and design of the study, acquisition, analysis and interpretation of data; all authors drafted the article and made critical revisions related to the intellectual content of the manuscript, and approved the final version of the article to be published.Institutional animal care and use committee statement: The Animal Care and Use Committee of the First Affiliated Hospital of Zhejiang Chinese Medicine University approved the protocol. Conflict-of-interest statement:To the best of our knowledge, no conflict of interest exists. METHODS:One hundred and twenty Wistar rats were randomly divided into two groups (60 in each group): Control group and Model group. The rats in each group were then randomly divided into three groups (20 in each group): C/M15, C/M25 and C/M40 (15, 25 and 40 represent the number of feeding weeks from termination). Rats in the control group received normal drinking water and rats in the model group received drinking water containing 100 μg/mL MNNG. Stomach tissues were collected at the end of the 15 th , 25 th and 40 th week, respectively, for microscopic measurement using hematoxylin and eosin staining. The expression of p-STAT3 and VEGF in different pathological types of gastric tissue, including normal, inflammation, atrophy, hyperplasia and gastric stromal tumor, was observed by immunohistochemistry and Western blot, and the corelation between p-STAT3 and VEGF was analyzed. RESULTS:(1) The expression of p-STAT3 in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor were significantly increased in the model group compared with the control group (2.5 ± 1.0, 2.75 ± Wang XY et al . 6.2 ± 0.45, 5.67 ± 0.55 vs 0.75 ± 0.36, P = 0.026, 0.035, 0.001, 0.002, respectively); the expression of p-STAT3 in tissue with dysplasia was higher than that in samples with gastritis or atrophy (6.2 ± 0.45 vs 2.5 ± 1.0, P = 0.006; 6.2 ± 0.45 vs 2.75 ± 0.36, P = 0.005, respectively); however, the expression of p-STAT3 in gastritis and atrophy was not significantly different (P > 0.05); (2) the expression of VEGF in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor was significantly increased in the model group compared with normal gastric mucosa; and the expression of VEGF in tissue with dysplasia was higher than that in tissue with inflammation and atrophy (10.8 ± 1.96 vs 7.62 ± 0.25, P = 0.029; 10.8 ± 1.96 vs 6.26 ± 0.76, P = 0.033, respectively); similarly, the expression of VEGF in tissue with gastritis and atrophy was not significantly different (P > 0.05); and (3) the expression of VEGF was positively correlated with p-STAT3.CONCLUSION: p-STAT3 plays an important role in gastric cancer formation by regulating the expression of VEGF to promote the progression of gastric tumor from gastritis.

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Expression of transforming growth factor alpha in experimental gastric carcinogenesis.

Abstract: The induction of adenocarcinomas in the glandular stomach of the adult male Wistar rat by N-methyl

Cited by 11 publications

References 13 publications

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

Attenuation by all-trans-retinoic acid of sodium chloride-enhanced gastric carcinogenesis induced by N-methyl-N ′-nitro-N-nitrosoguanidine in Wistar rats

Differential distribution of transforming growth factor-a immunohistochemistry within whole gastric mucosa in rats

Expression of p-STAT3 and vascular endothelial growth factor in MNNG-induced precancerous lesions and gastric tumors in rats

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